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Block 6 Week 2 > Hypersensitivity Type III- Hunter > Flashcards

Hypersensitivity Type III- Hunter Flashcards

1
Q

What is type III hypersensitivity driven by?

A

IgG, immune complexes, complements and phagocytes

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2
Q

What is an example of a type III hypersensitivity response?

A

serum sickness, systemic lupus erythematosus

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3
Q

What can cause immune complex diseases?

A

microbial antigens
drugs and biologics
molds, spores, chemicals
self antigens

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4
Q

What determines the pathology of a type III hypersensitivity reaction?

A

dose and route

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5
Q

What will a high dose intravenously of an antigen cause?

A

vasculitis
nephritis
arthritis

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6
Q

What will a subcutaneous dose of an antigen cause?

A

arthus reaction

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7
Q

What will an inhaled dose of an antigen cause?

A

farmer’s lung

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8
Q

What is an arthrus reaction?

A

a local type III hypersensitivity reaction

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9
Q

What kind of immune complex problem is this:
with microbial antigens such as streptococcal infections, malaria, and viral hepatitis can overwhelm the system that rids the body of immune complexes leading to deposition of excess immune complexes into blood vessels and tissues.

A

persistent infection

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10
Q

What kind of immune complex problem is this:

drugs and biologics form acute immune complex disease which can lead to the arthus reaction and serum sickness

A

injected antigen

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11
Q

What kind of immune complex problem is:
molds, spores and chemical and lead to immune complexes and hypersensitivity pneumonitis (extrinsic allergic alveolitis) this:

A

inhaled antigen

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12
Q

What kind of immune complex problem is this:
self-antigens are bound by antibodies forming complexes and lead to chronic disease like that seen in systemic lupus erythematosis, and rheumatoid arthritis

A

autoimmunity

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13
Q

How do you clear an immune complex?

A

The C3b/C4b found on immune complexes will bind CR1 on RBCs and be taken to the liver or spleen to be cleared.

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14
Q

What does the C3b/C4b on immune complexes bind to on the RBC?

A

CR1

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15
Q

What destroys immune complexes in the spleen?

A

splenic macrophages

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16
Q

What destroys immune complexes in the liver?

A

kupffer cells

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17
Q

What do kupffer cells and splenic macrophages have on them to allow them to bind and destroy immune complexes?

A

FC receptors

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18
Q

Do the RBCs attached to the immune complexes get destroyed as well?

A

no they are safe and return to the circulation.

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19
Q

(blank) factors influence immune complex deposition.

A

hemodynamic

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20
Q

Deposition of immune complexes in blood vessel walls leads to (blank)

A

immunopathology

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21
Q

Where do immune complexes deposit in the vasculature?

A

in between endothelial cells

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22
Q

When immune complexes deposit in the vasculature, what is activated?

A

complement releasing anaphylatoxins (C5a and C3a)

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23
Q

So once a immune complex deposits in between endothelial cells and anaphylatoxin (C5a and C3a) are activatd what happens next?

A

neutrophils are recruited to the site and bind immune complexes by their Fc receptors and become activated. The neutrophils attempt to phagocytize the complex but cant so they release a bunch of granules, inflammatory mediators, and enzymes to cause tissue destruction.

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24
Q

What is the most common post-infectious actue proliferative nephritis?

A

post-streptococcal glomerulonephritis

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25
Q

Patients with post-streptococcal glomerulonephritis present with what 2 things?

A

hematuria and proteinuria

26
Q

WHen you see a lumpy bumpy glomerulus, what should you be thinking?

A

deposition of complement

27
Q

How can you induce the arthus reaction?

A

locally inject antigen in an immune individual w/ lots of pre-existing IgG antibody to the antigen-> local immune complex formation-> activation of FcgammaR3 on mast cells induces their degranulation-> local inflammation, increased fluid and protein release, phagocytosis and blood vessel occlusion

28
Q

Local injection of antigen in individuals with high levels of pre-existing antibodies can cause the (blank) reaction

A

arthus reaction

29
Q

FCepsionRI receptors on mast cells, basophils, activated eosinophils have this receptor to do what?

A

to release their stuff in response to IgE!!!!

30
Q

FCgammaRIII receptors on mast cells respond to what and do what?

A

IgG immune complexes and degranulate

31
Q

(blank) form in the setting of high local concentration of vaccine antigens and high circulating antibody concentrations.

A

immune complexes

32
Q

A local vasculitis is associated with deposition of (blank) and (blank)

A

immune complexes and complement activation

33
Q

What are these symptoms of:

severe pain, swelling, induration, edema, hemorrhage, and occasionally necrosis.

A

arthrus reaction

34
Q

when does an arthrus reaction typically occur after a vaccine?

A

4-12 hours after vaccination

35
Q

What is the mechanism behind penicillin-induced serum sickness?

A

the chemically reactive penicilloyl moiety binds to self proteins and induces an antibody response, IgG anti-peniciliin antibodies form immune complexes with penicilin-> complement activation releases C3a which causes hitamine release from mast cell and urticaria (hives).

36
Q

What is extrinsic allergic alveolitis (hypersensitivity pneumonitis)?

A

immune complexes with inhaled fungal antigens (farmer’s lung-bird fancier’s disease)

37
Q

What involves the development of IgG antibodies to inhaled mold that form immune complexes?

A

Extrinsic allergic alveoitis

38
Q

Why are immune complexes so sucky?

A

because they fix complement and release anaphylatoxns causes local inflammation.

39
Q

Acute exacerbations of extrinsc allergic alveolitis can be treated by what?

A

corticosteroids

40
Q

What is type IV hypersensitivity (delayed type hypersensitivity) caused by?

A

Th17 cells, Th1 cells, Th2 cells

41
Q

The Th1 delayed type hypersensitivity (DTH) response is orchestrated by (blank) produced by macrophages; T cells make IFN-gamma that further activates (blank)

A

IL-12

macrophages

42
Q

The TH17 delayed hypersensitivity reaction is driven by (blank) and (blank) produced by macrophages. T cells make (blank) and (blank) that recruit and activate neutrophils

A

IL-23 and TGF-beta

IL-17 and IL-22

43
Q

WHat does IL-17 and IL-22 do?

A

recruit and activate neutrophils

44
Q

What is the TH17 DHT reaction driven by?

A

IL-23 and TGF-beta

45
Q

The (blank) response involves cytoxocity and is a component of several autoimmune diseases like Type I diabetes

A

CD8 DTH response

46
Q

CD8 makes what cytokine?

A

IFN-gamma

47
Q

So describe the whole type IV hypersensitivity (delayed type hypersensitivity) response?

A

IL-12 released from macrophages makes Th1 which releases IFN gamma and TNG that further activates macrophages
THEN
IL-23 and TGF-beta produced by macrphages triggers T cells to make IL-17 and IL-22 that recruit and activates neutrophils
THEN
CD8s release IFN gamma and kill shit

48
Q

Why do you get the wheel and flare when you get a TB shot?

A

Antigen is injectin into subcutaneous tissue and the antigen is processed by APCs and then TH1 cells recognized the antigen and release cytokines onto vascular endothelium which will recruit phagocytes and plasma to site of antigen injection and causes visible lesion

49
Q

T cell-mediated reactions are called DTH because they take (blank) hours to mature

A

24-72 hours

50
Q

What is allergic contact dermitis caused by?

A

CD4 or CD8 T cells

51
Q

Explain how allergic contact dermatitis is caused

A

small highly reactive molecules penetrate skins-> create haptens-> haptens are presented by MHC molecules-> Langerhan dendritic cells take up and process antigen, these migrate to lymph nodes and activate T cells.-> The memory T cells migrate to the dermis->Then an approximate exposure triggers memory T cells which release IFN-gamma. IFN-gamma sitmulates keratinocytes to release cytokines and chemokines that enhance inflammatory rsponse by recruiting and activating monocytes

52
Q

In allergic contact dermatitis, what does IFN-gamma stimulate?

A

Keratinocytes to release cytokine and chemokines

53
Q

In type IV hypersensitivity to a contact sensitiizing agent

Hapten binds self protein in the skin and is pinocytosed by (blank) and are present in (bank) molecules to (blank) cells

A

dendritic cells
MHC class II
CD4 T cells

54
Q

In type IV hypersensitivity to a contact sensitiizing agent, previously sensitized (Blank) cells interact with langerhan dendritic cells

A

T cell

55
Q

In type IV hypersensitivity to a contact sensitiizing agent, (bank) stimulates keratinocyes to make cytokines and chemokines.

A

IFN-gamma

56
Q

In type IV hypersensitivity to a contact sensitiizing agent, IFN-gamma stimulates keratinocytes to make cytokines and chemokines which wil attract what cels to the site?

A

mononuclear cells

57
Q

What happens upon second exposure of poison ivy?

How do you treat it?

A

severe reaction triggered by memory T cells result in contact dermatitis and epidermal blisters with dermal and epidermal mononuclear infiltrates.

systemic corticosteroids

58
Q

Explain nickel dermatitis

A

chemically reactive metals like nickle bind to host proteins and activate T cells-> T cels release IFN-gamma which activate keratinocytes-> active keratinocytes release mediates that cause mononuclear infiltrate of dermis.

59
Q

What kind of hypersensitivity is acrylate and latex?

A

Type IV hypersensitivity

60
Q

What does IFn gamma really do?

A

brings in macrophages.

Block 6 Week 2 (7 decks)

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